Cyanide (FINAL) Flashcards
Which species are most likely to get cyanide poisoning?
Large animals
What are possible sources of cyanide poisoning in large animals?
- Ingestion of cyanogenic plants
- Wild cherry (Prunus spp)
- Sudan grass, Johnson grass, and sorghums
What does sudan grass, Johnson grass, and sorghum contain?
Cyanogenic glycosides that can liberate toxic amounts of HCN
What species is this?
Chokecherry (Prunus spp)
What is this?
Sorghums (Sorghum spp)
What can be a source of cyanide poisoning in small animals?
Hydrogen cyanide and cyanide salts have many uses that lead to poisoning in small animals
What is used as a fumigant rodenticide that can cause poisoning in small animals?
Hydrogen cyanide gas
What compound do some fertilizers contain that is toxic to small animals?
Cyanamide
T/F: Sodium nitroprusside is used as a hypotensive
TRUE
Combustion of what produces HCN gas that can poison small animals?
Many plastic compounds
What are some cyanogenic plants that cause toxicity in small animals?
-
Prunus spp
- Cherries, apples, plums, apricots
- Some species of lima bean and cassava roots (tapioca)
What is cyanide also known as?
Hydrogen cyanide (HCN), hydrocyanic acid, or prussic acid
Is HCN a volatile gas?
YES
T/F: HCN will disappear as the plant dries and also from the rumen contents
TRUE
What is HCN’s characteristic odor?
Bitter almond or ammoniacal
Is HCN an irritant to mucous membranes
Of course it is
What does the CN- radical form?
Complexes with a number of chemicals, such as ferric ion, cupric, and molybdenum
Does cyanide have an antithyroid effect?
No–thiocyanate SCN has an antithyroid effect
What are the toxic levels of cyanide?
Greater than 200ppm in the plant is toxic
What is the acute oral MLD of HCN?
2-2.3 mg/kg in all species
Which species are more/less susceptible to cyanide toxicosis?
- Ruminants are more susceptible than horses and swine
- Sheep are less susceptible than cattle
Why are ruminants more susceptible to HCN poisoning?
Hydrolysis by the rumen microflora causes release of cyanide from cyanogenic plants
What happens to cyanogenic plants when damaged?
- Plant damage (stunting, wilting, trampling, frost, drought, or treatment w/ 2,4-D herbicides)
- Causes release of beta-glucosidase that causes hydrolysis of cyanogenic glycosides and release of cyanide (HCN)
What is the order of cyanogenic glycoside concentrate in plant parts?
Seeds > leaves > bark > stems > fruit
Which plant stage contains more glycoside?
Young/growing
What soil condition might increase cyanide poisoning?
High N or low P–may increase glycoside
T/F: Plants can contain large amounts of free HCN and cyanogenic glycoside
TRUE
T/F: Rapid ingestion and ingestion of large portions of a cyanogenic plant can cause toxicosis
TRUE
Where is HCN absorbed from?
HCN is rapidly absorbed from the GI tract, by inhalation, and from intact skin
Where is HCN distributed?
Throughout the whole body
Where is CN- metabolized?
In the presence of thiosulfate, CN- is metabolized by serum and liver sulfurtransferase (rhodanese) to thiocyanate (SCN-) which is relatively less toxic and is excreted in the urine
Excretion of HCN?
Small amounts are excreted in the urine or expired air
What happens to excess CN- in tissues/blood?
It binds with ferric iron and cupric copper of the mitochondrial cytochrome oxidase
–> this blocks electron transport and inhibits the cells from utilizing available oxygen –> histotoxic anoxia particularly in the brain
Does CN- toxicosis respond to oxygen therapy
NO–cells can’t utilize the available oxygen
T/F: Anaerobic glycolysis leads to metabolic acidosis in HCN toxicosis
TRUE
What might cyanide inhibit following toxicosis?
May inhibit enzymes of glycolysis and citric acid cycle and decrease cellular energy
What effect does cyanide have?
A prominent vasoconstrictor effect
Does HCN toxicosis cause neuronal damage?
Yes, due to histotoxic anoxia
What occurs following chronic HCN toxicity?
- Neuronal degeneration and demyelination of the spinal cord and brain
- Low levels of cyanide are goitrogenic due to thiocyanate
T/F: Both peracute and acute poisoning can have an extremely rapid onset
TRUE
T/F: Animals may die from poisoning without manifesting clinical signs
TRUE
What are the clinical signs of acute poisoning?
- Signs occur in rapid succession and include tachypnea, apparent anxiety, severe panting, gasping, and behavioral alarm
- Other signs may be muscle tremors, salivation, lacrimation, urination, defecation, severe colic, vomiting, prostration, bright red mucous membranes (from hyperoxygenation of the blood), clonic convulsions, and rapid death
T/F: Signs of acute HCN poisoning will vary among species
FALSE–signs are similar in all species
How long does it take for animals to die from acute poisoning?
About 4-5min from onset of clinical signs
What are the clinical signs of chronic poisoning?
- Posterior paralysis, urinary incontinence and cystitis, which may result in infection
- Constipation due to lower spinal cord degeneration
- May have goitrogenic effect
Which sample is positive for cyanide poisoning?
Far left
What are the lesions associated with cyanide toxicosis?
- Bright red mm, cherry-red blood that may not clot or will slowly clot
- GI tract and lungs show congestion and petechial hemorrhages
- Plants may be seen in rumen contents
- May be smell of cyanide, although it leaves the rumen contents rapidly
What specimens are used for chemical analysis?
What should be done to the specimens?
- Forage (200ppm considered toxic), blood (stays longer than in tissues), rumen contents, liver, muscle, brain, and heart (if taken w/in 4hrs of death)
- Brain and heart are good specimens
- All specimens (except blood) should be frozen immediately and kept frozen until analysis
What can be used as a preservative for plant specimens?
Adding 1-3% solution of mercuric chloride–prevents hydrolysis
Is chemical analysis useful for emergency situations?
No–results take days
What is elevated on the lab diagnosis?
- Elevated thiocyanate levels in urine
- Lactic acidosis and increased anion gap
- Good indicators for presence and severity of cyanide poisoning
What is the sodium picrate paper test?
- Commercial kit test to detect toxic levels of cyanide in the rumen contents or plant
- Yellow color changes to brick red in a few minutes (in airtight glass jar)
Diagnosis?
- History of consuming cyanogenic plants, bright red mm, and odor of cyanide are indicative of cyanide toxicosis
- Chemical analysis confirms diagnosis
DDx?
- Carbon monoxide (causes bright red blood)
- Hydrogen sulfide
- Nitrate
- Urea
How can you differentiate between cyanide toxicosis and hydrogen sulfide poisoning?
H2S causes rapid death by inhibition of cytochrome oxidase, but blood and tissues will be dark
How can you differentiate between nitrate and cyanide toxicity?
Nitrate can cause rapid death (with little exposure), but the blood is chocolate brown colored
How is urea poisoning similar/different from cyanide poisoning?
Urea may cause rapid death with few lesions, but causes severe colic, nervous and behavioral effects, and the odor of ammonia in the rumen
Treatments?
- Sodium nitrite 20% IV at 10-20mg/kg
- Sodium thiosulfate orally
- Oxygen therapy is beneficial in addition to nitrite-thiosulfate
- Vinegar (4L) in 12-20 L cold water orally to slow microbial hydrolysis
- Mineral oil as a laxative
How does sodium nitrite work as a treatment?
- 20% IV at 10-20mg/kg
- Immediately improves perfusion by causing vasodilation
- Causes methemoglobin which can bind the CN- and reactivate cytochrome oxidase (too slow to account for the rapid improvement)
How does sodium thiosulfate work as treatment?
- 20% IV at 600mg/kg (?)
- Converts CN- to thiocyanate (SCN) which is less toxic and is excreted in urine
